Neutral sphingomyelinase‐2 and cardiometabolic diseases
| Autor: | Yat Hei Leung, Rasheed Ahmad, Fahd Al-Mulla, Sardar Sindhu, Marc Prentki, Hossein Arefanian, S.R. Murthy Madiraju |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Ceramide
Endocrinology Diabetes and Metabolism 030209 endocrinology & metabolism Inflammation Type 2 diabetes Ceramides Proinflammatory cytokine 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Insulin resistance medicine Humans ceramide 030212 general & internal medicine Sphingolipids business.industry Public Health Environmental and Occupational Health Obesity Comorbidity/Etiology and Pathophysiology Atherosclerosis medicine.disease Sphingolipid 3. Good health Sphingomyelin Phosphodiesterase nSMase2 Diabetes Mellitus Type 2 chemistry Immunology sphingolipid Metabolic syndrome medicine.symptom cardiometabolic diseases Sphingomyelin business |
| Zdroj: | Obesity Reviews |
| ISSN: | 1467-789X 1467-7881 |
| DOI: | 10.1111/obr.13248 |
| Popis: | Summary Sphingolipids, in particular ceramides, play vital role in pathophysiological processes linked to metabolic syndrome, with implications in the development of insulin resistance, pancreatic ß‐cell dysfunction, type 2 diabetes, atherosclerosis, inflammation, nonalcoholic steatohepatitis, and cancer. Ceramides are produced by the hydrolysis of sphingomyelin, catalyzed by different sphingomyelinases, including neutral sphingomyelinase 2 (nSMase2), whose dysregulation appears to underlie many of the inflammation‐related pathologies. In this review, we discuss the current knowledge on the biochemistry of nSMase2 and ceramide production and its regulation by inflammatory cytokines, with particular reference to cardiometabolic diseases. nSMase2 contribution to pathogenic processes appears to involve cyclical feed‐forward interaction with proinflammatory cytokines, such as TNF‐α and IL‐1ß, which activate nSMase2 and the production of ceramides, that in turn triggers the synthesis and release of inflammatory cytokines. We elaborate these pathogenic interactions at the molecular level and discuss the potential therapeutic benefits of inhibiting nSMase2 against inflammation‐driven cardiometabolic diseases. |
| Databáze: | OpenAIRE |
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